Exam 2: Inflammation & Immunity Flashcards
(53 cards)
Acute inflammation
minutes to several days; presence of neutrophils
Phases:
1. Vascular: increase in blood flow and changes in small blood vessels (minimize damages)
- Cellular: migration of leukocytes or white blood cells (WBCs) for tissue repair (Leukocyte activation and phagocytosis)
Chronic inflammation
days to years; presence of lymphocytes, macrophages, fibrosis tissue
Purpose of inflammation
eliminate cause of cell injury, remove damaged tissue, and generate new tissue
Clinical manifestations of inflammation
Cardinal: Redness, warmth, swelling, tenderness/pain, loss of function
Systemic response: Temperature, elevated C-reactive protein (CRP), elevated erythrocyte sedimentation rate (ESR), elevated white blood cells (WBCs), malaise and anorexia, lymphadenitis
Endothelial cells
release platelet and thrombotic cell agents to form a clot, regulates synthesis and release of inflammatory mediators
Platelets
circulating in blood to help form clots and release potent inflammatory mediators
Mast cells
when activated stimulate release of histamine, TNF-α, Interleukins, cytokines, monocytes, macrophages
Histamine 1
released from mast cells
- Vasodilation
- Vascular permeability
- Bronchoconstriction
**Histamine 2 causes increased secretion of gastric acid
Prostaglandins
group of lipids with hormone-like actions that your body makes primarily at sites of tissue damage or infection
- Increased vascular permeability
- Vasodilation
- Fever
- Pain
- Neutrophil chemotaxis (The attractive forces that pull the Phagocytes to the site of injury/infection)
Leukotrienes
Released by mast cells
Think of asthma attack ->
* Increased vascular permeability
* Smooth muscle contraction which promotes bronchoconstriction and airway edema
Promotes slower and more prolonged responses than Histamine
Cytokines
Chemokines: family of small proteins that act primarily as chemoattractant to recruit and direct the migration of immune and inflammatory cells
Interleukins (ILs)
Interferons (IFNs)
Tumor necrosis factor alpha (TNF-α)
Flow chart of inflammation process
Exudate
a mass of cells and fluid that has seeped out of blood vessels or an organ, especially in inflammation.
Ulceration
a site of inflammation that has become necrotic or eroded
Serous
watery fluid, amber/clear
Hemorraghic or sanginous
red blood cells, red/pink
Fibrinous
increased fibrinogen and form a thick sticky meshwork
Purulent
pus, degraded white blood cells, proteins, and tissue debris
yellow/white/green
dendritic cells
innate cells that capture, process, and present antigens to adaptive immune cells and mediate their polarization into effector cells
link b/t innate and adaptive along with cytokines
antigen
a substance that induces the formation of antibodies because it is recognized by the immune system as a threat
Humoral immunity
B cells use antibodies to tag pathogens for destruction
immunoglobulins
substances found in the “humors” (fluid) of the body
Innate immunity:
It is the body’s first and immediate line of defense; includes macrophages, cytokines and natural killer cells. Composed of the body’s natural anatomical barriers, normal flora, white blood cells (WBCs), and protective enzymes and chemicals. Macrophages phagocytose foreign debris and antigens. Interferons, cytokines, and hydrochloric acid are some of the protective enzymes and chemicals.
Adaptive immunity:
after the innate system and more specific protection
developed after exposure to antigens and act rapidly, specifically, destructively, and with memory for every individual antigen it has encountered through human cell surface antigens called major histocompatibility complexes (MHCs), also called human leukocyte antigens (HLAs)
allows the body to distinguish between antigens that belong to the host versus antigens that are from an invader
Active acquired Immunity:
Obtained through exposure to an antigen or through immunization (vaccine). The patient’s body has to synthesize specific immunoglobulins against an antigen